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Important casual association of carotid body and glossopharyngeal nerve and lung following experimental subarachnoid hemorrhage in rabbits. First report

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Erişim

info:eu-repo/semantics/closedAccess

Tarih

2014

Yazar

Yolaş, Coşkun
Kanat, Ayhan
Aydın, Mehmet Dumlu
Türkmenoğlu, Osman Nuri
Gündoğdu, Cemal

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Künye

Yolas, C., Kanat, A., Aydin, M.D., Turkmenoglu, O.N., Gundogdu, C. (2014). Important casual association of carotid body and glossopharyngeal nerve and lung following experimental subarachnoid hemorrhage in rabbits. First report. Journal of the Neurological Sciences, 336(1-2), 220-226. https://doi.org/10.1016/j.jns.2013.10.047

Özet

Object: the glossopharyngeal nerves (GPNs) and carotid bodies (CBs) have an important role in the continuation of the cerebral autoregulation and cardiorespiratory functions. the relationship between degenerative injury of CB and the GPN in subarachnoid hemorrhage (SAH) was studied. Methods: Twenty rabbits were included in this study. Five of them (n = 5) were used as control group. the remaining animals (n = 15) were exposed to experimental SAH. in the six animals of the SAH group, severe signs of illness were observed, and these six animals were killed in the first week after SAH. Others animals (n = 9) were followed for 20 days and then sacrificed. GPNs and CBs were examined and, the live and degenerated GPN axon number, and of CB neuron numbers were stereologically estimated. Results: the mean number of live neurons in CBs was 4206.67 +/- 148.35 and live axons of GPNs were 1211.66 +/- 14.29 in the animals of the control group. the number of degenerated neurons of CBs was 2065 +/- 110.27 and the number of degenerated axons of GPNs was 530.83 +/- 43.48 in early killed animals with SAH. the number of degenerated neurons of CBs and the number of degenerated axons of GPNs were found as 1013.89 +/- 4184 and 2270.5 +/- 13438 in the living animals with SAH, respectively. Conclusions: High number of degenerated axons of GPN and neurons of CBs of the early killed animals suggest that the mortality in early SAH might be due to GPNs injury secondary to compression of their axons or supplying vessels by the probably herniated brainstem, and secondary denervation injury of CBs, and lung. Crown Copyright (c) 2013 Published by Elsevier B.V. All rights reserved.

Kaynak

Journal of the Neurological Sciences

Cilt

336

Sayı

01.Feb

Bağlantı

https://doi.org/10.1016/j.jns.2013.10.047
https://hdl.handle.net/11436/3176

Koleksiyonlar

  • PubMed İndeksli Yayınlar Koleksiyonu [2440]
  • Scopus İndeksli Yayınlar Koleksiyonu [5917]
  • TF, Cerrahi Tıp Bilimleri Bölümü Koleksiyonu [1215]
  • WoS İndeksli Yayınlar Koleksiyonu [5260]



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